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甘草甜素可改善果糖诱导的大鼠代谢综合征X模型中的胰岛素抵抗、高血糖、血脂异常和氧化应激。

Glycyrrhizin ameliorates insulin resistance, hyperglycemia, dyslipidemia and oxidative stress in fructose-induced metabolic syndrome-X in rat model.

作者信息

Sil Rajarshi, Ray Doel, Chakraborti Abhay Sankar

机构信息

Department of Biophysics, Molecular Biology and Bioinformatics, University College of Science, University of Calcutta, 92 Acharyya Prafulla Chandra Road, Kolkata 700 009, India.

出版信息

Indian J Exp Biol. 2013 Feb;51(2):129-38.

PMID:23923606
Abstract

This study investigates if glycyrrhizin, a constituent of licorice (Glycyrrhiza glabra) root, is able to treat the complications (insulin resistance, hyperglycemia, dyslipidemia and oxidative stress) of metabolic syndrome. Metabolic syndrome was induced in rats by feeding a fructose-enriched (60%) diet for six weeks, after which single dose of glycyrrhizin (50 mg/kg body weight) was administered intraperitoneally. Different biochemical parameters from blood were estimated during three weeks after treatment. Then the rats were sacrificed to collect skeletal muscle tissue. Glycyrrhizin reduced the enhanced levels of blood glucose, insulin and lipids in metabolic syndrome group. Increased advanced glycation end products of hemoglobin, glycohemoglobin, hemoglobin-mediated iron release and iron-mediated free radical reactions (arachidonic acid and deoxyribose degradation) in metabolic syndrome were inhibited by glycyrrhizin treatment. Reduced activities of enzymatic antioxidants (superoxide dismutase and catalase) and elevated oxidative stress markers (malonaldehyde, fructosamine, hemoglobin carbonyl content and DNA damage) in metabolic syndrome were reversed to almost normal levels by glycyrrhizin. The decreased levels of peroxisome proliferator activated receptor gamma (PPARgamma) and glucose transporter 4 (GLUT4) proteins in skeletal muscle of metabolic syndrome group were elevated by glycyrrhizin, indicating improved fatty acid oxidation and glucose homeostasis.

摘要

本研究调查了甘草(Glycyrrhiza glabra)根的成分甘草酸是否能够治疗代谢综合征的并发症(胰岛素抵抗、高血糖、血脂异常和氧化应激)。通过给大鼠喂食富含果糖(60%)的饮食六周诱导代谢综合征,之后腹腔注射单剂量的甘草酸(50毫克/千克体重)。在治疗后的三周内评估血液中的不同生化参数。然后处死大鼠以收集骨骼肌组织。甘草酸降低了代谢综合征组中升高的血糖、胰岛素和脂质水平。甘草酸治疗抑制了代谢综合征中血红蛋白晚期糖基化终产物、糖化血红蛋白、血红蛋白介导的铁释放和铁介导的自由基反应(花生四烯酸和脱氧核糖降解)的增加。甘草酸将代谢综合征中酶促抗氧化剂(超氧化物歧化酶和过氧化氢酶)活性的降低以及氧化应激标志物(丙二醛、果糖胺、血红蛋白羰基含量和DNA损伤)的升高逆转至几乎正常水平。甘草酸提高了代谢综合征组骨骼肌中过氧化物酶体增殖物激活受体γ(PPARγ)和葡萄糖转运蛋白4(GLUT4)蛋白的降低水平,表明脂肪酸氧化和葡萄糖稳态得到改善。

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